ADAR1 entraps sinister cellular dsRNAs, thresholding antiviral responses

Trends Immunol. 2021 Nov;42(11):953-955. doi: 10.1016/j.it.2021.09.013. Epub 2021 Oct 9.

Abstract

ADAR1 edits adenosines to inosines in cellular double-stranded (ds)RNA, thereby preventing aberrant activation of antiviral dsRNA sensors, as well as interferon (IFN) induction in Aicardi-Goutières syndrome (AGS) encephalopathy. Recently, Nakahama et al., Tang et al., Maurano et al., and de Reuver et al. demonstrated that Adar1 Zα domain-mutant mice show aberrant MDA5 and PKR activation, developing encephalopathies; short Z-RNA patches within cellular dsRNA are unexpectedly crucial in causing aberrant antiviral responses.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Deaminase* / genetics
  • Adenosine Deaminase* / metabolism
  • Animals
  • Antiviral Agents
  • Autoimmune Diseases of the Nervous System* / genetics
  • Humans
  • Mice
  • RNA Editing
  • RNA, Double-Stranded

Substances

  • Antiviral Agents
  • RNA, Double-Stranded
  • ADAR1 protein, mouse
  • Adenosine Deaminase